Somatostatin, insulin, and glucagon secretion from isolated perfused pancreas of obese rats

1981 ◽  
Vol 241 (2) ◽  
pp. E146-E150
Author(s):  
S. Seino ◽  
Y. Seino ◽  
J. Takemura ◽  
K. Tsuda ◽  
H. Kuzuya ◽  
...  

A comparison of the somatostatin with the insulin and glucagon secretions in hypothalamic obesity and genetic obesity was made using the isolated perfused pancreas of rats. In our perfusion experiment, the somatostatin response to 19 mM arginine in the presence of 4.4 mM glucose was significantly greater in both ventromedial hypothalamus (VMH)-lesioned and Zucker fa/fa rats than in their controls, as was the perfusate insulin. The perfusate arginine-stimulated glucagon secretion appeared no different in obese and control rats. Because hyperinsulinemia in vivo and hyperresponses to arginine of perfusate insulin and somatostatin were observed in both VMH-lesioned and Zucker fa/fa rats, whereas the perfusate glucagon secretion in the presence of 4.4 mM glucose was unchanged by obesity, the secretory behavior of some pancreatic hormones seems similar in VMH-lesioned and Zucker fa/fa rats in certain conditions. These results suggest that some abnormalities of pancreatic hormone secretion may be caused by a mechanism common to obesity, whether caused experimentally or genetically.

1986 ◽  
Vol 250 (6) ◽  
pp. E669-E676 ◽  
Author(s):  
C. I. Edwards ◽  
R. J. Howland

Arginine-stimulated insulin and glucagon outputs from isolated perfused pancreata of warm-acclimated and 2-, 4-, and 6-wk cold-acclimated rats (4 degrees C) were determined to assess whether observed changes in these parameters were a result of cold exposure per se or a part of the adaptive process of cold acclimation. Progressive and sequential changes were seen in both insulin and glucagon outputs. At 2 wk cold acclimation, glucagon rose and insulin output tended to fall, at 4 wk, glucagon output remained elevated and insulin output was further reduced, and at 6 wk, glucagon output had returned to control levels, whereas insulin output was substantially further reduced. These changes resulted in reduction of the insulin-to-glucagon molar ratio of the total arginine-induced output from 7.27 +/- 1.76 (SE) in the warm acclimate to 2.31 +/- 0.79 (SE) at 2 wk, 1.42 +/- 0.29 (SE) at 4 wk, and 1.26 +/- 0.21 (SE) at 6 wk cold acclimation. The data do not provide in vitro support for the hypothesis that changes in pancreatic hormone secretion in vivo are a consequence of cold exposure and not cold acclimation.


1996 ◽  
Vol 81 (6) ◽  
pp. 2528-2533 ◽  
Author(s):  
Fethi Trabelsi ◽  
Jean-Marc Lavoie

Trabelsi, Fethi, and Jean-Marc Lavoie. Arginine-induced pancreatic hormone secretion during exercise in rats. J. Appl. Physiol. 81(6): 2528–2533, 1996.—The aim of the present investigation was to 1) determine whether arginine-induced pancreatic hormone secretion can be modified during an exercise bout, and 2) verify whether the sectioning of the hepatic branch of the vagus nerve can alter the arginine-induced insulin and glucagon secretion during exercise in rats. To this end, we studied the effects of an intraperitoneal injection of arginine (1 g/kg body mass) during an exercise bout (30 min, 26 m/min, 0% grade) on the pancreatic hormone responses. These effects were determined in one group of sham-operated exercising rats and compared with three control groups: one group of resting rats, one group of saline-injected exercising rats, and one group of hepatic-vagotomized exercising rats. Five minutes after the injection of arginine, significant ( P < 0.05) increases in insulin, glucagon, and C-peptide concentrations were observed in exercising as well as in resting rats. These responses were not, however, altered by the hepatic vagotomy and/or by the exercise bout. It is concluded that arginine is a potent stimulus of pancreatic hormone secretion during exercise, even though the sympathoadrenal system is activated. These results also indicate that a hepatic vagotomy does not seem to influence arginine-induced hormonal pancreatic responses and question the role of the putative hepatic arginoreceptors in the control of the pancreatic hormone secretion during exercise.


1994 ◽  
Vol 86 (3) ◽  
pp. 311-316 ◽  
Author(s):  
Dr Hiroshi Hirose ◽  
Hiroshi Maruyama ◽  
Koichi Kido ◽  
Katsuhiko Ito ◽  
Kazunori Koyama ◽  
...  

1. The effects of various stimuli, including changes in glucose concentration, arginine, tyramine and noradrenaline, on insulin and glucagon secretion were investigated using isolated perfused pancreata of obese and lean male Zucker rats at 12 months of age. 2. In Zucker fatty rats, the insulin secretion rate was significantly (P < 0.01) higher than that of lean rats at all glucose concentrations tested (8.3, 16.7 and 1.4 mmol/l). However, the integrated insulin secretory response to raising the glucose concentration from 8.3 to 16.7 mmol/l was almost absent in these rats. The glucagon secretion rates were significantly lower at 8.3 and 1.4 mmol/l glucose (P < 0.001 for both), and in responses to 10 μg/ml tyramine and 0.1 μmol/l noradrenaline (P < 0.05 for both), in Zucker fatty rats. Integrated insulin and glucagon responses to 10 mmol/l arginine were identical in the two groups. 3. Histopathological and immunochemical studies revealed hyperplasia of β-cells and scattered α-cells in the enlarged islets of Zucker fatty rats. 4. These results suggest that, in Zucker fatty rats, the decreased glucagon secretion in the isolated perfused pancreas is attributable to changes in the environment of α-cells and/or the inhibitory effects of hypersecreted insulin.


2003 ◽  
Vol 81 (7) ◽  
pp. 720-729 ◽  
Author(s):  
Nobuharu Yamaguchi ◽  
Tamar Rita Minassian ◽  
Sanae Yamaguchi

The aim of the present study was to characterize the effects of pituitary adenylate cyclase activating polypeptide (PACAP) on the endocrine pancreas in anesthetized dogs. PACAP1–27 and a PACAP receptor (PAC1) blocker, PACAP6–27, were locally administered to the pancreas. PACAP1–27 (0.005–5 μg) increased basal insulin and glucagon secretion in a dose-dependent manner. PACAP6–27 (200 μg) blocked the glucagon response to PACAP1–27 (0.5 μg) by about 80%, while the insulin response remained unchanged. With a higher dose of PACAP6–27 (500 μg), both responses to PACAP1–27 were inhibited by more than 80%. In the presence of atropine with an equivalent dose (128.2 μg) of PACAP6–27 (500 μg) on a molar basis, the insulin response to PACAP1–27 was diminished by about 20%, while the glucagon response was enhanced by about 80%. The PACAP1–27-induced increase in pancreatic venous blood flow was blocked by PACAP6–27 but not by atropine. The study suggests that the endocrine secretagogue effect of PACAP1–27 is primarily mediated by the PAC1 receptor, and that PACAP1–27 may interact with muscarinic receptor function in PACAP-induced insulin and glucagon secretion in the canine pancreas in vivo.Key words: atropine, PACAP, PAC1, muscarinic, interaction.


1986 ◽  
Vol 134 (3) ◽  
pp. 1291-1297 ◽  
Author(s):  
R.A. Silvestre ◽  
P. Miralles ◽  
P. Moreno ◽  
M.L. Villanueva ◽  
J. Marco

1988 ◽  
Vol 117 (3) ◽  
pp. 302-306 ◽  
Author(s):  
Lise D. Wogensen ◽  
Thomas Mandrup-Poulsen ◽  
Helle Markholst ◽  
Jens Mølvig ◽  
Åke Lernmark ◽  
...  

Abstract. The acute effects of recombinant human interleukin-1 beta (rIL-1) on basal and glucose-stimulated insulin release were investigated in the isolated perfused pancreas. At a concentration of 20 μg/l rIL-1 had no effect on basal insulin release, but increased the total amount of insulin released during first and second phase insulin release in response to 20 mmol/l D-glucose in the rat pancreas (P < 0.05). In addition, 26 μg/l of rIL-1 potentiated insulin release in response to square wave infusions of stimulatory concentrations of glucose (11 mmol/l) in the porcine pancreas. We hypothesize that IL-1 in the systemic circulation may affect B cell function in vivo.


1991 ◽  
Vol 260 (1) ◽  
pp. E59-E66 ◽  
Author(s):  
J. W. Starnes ◽  
E. Cheong ◽  
F. M. Matschinsky

This is the first study investigating hormone secretion by the isolated perfused pancreas of the aged Fischer 344 rat. Nutrient-induced release of insulin, glucagon, and somatostatin in overnight-fasted rats aged 2, 10, 18, 24, and 30 mo was studied. After an equilibration period, the pancreas was perfused for 20 min with buffer A (containing 4.2 mM glucose plus a 3.5 mM mixture of amino acids) then for 20 min with buffer B (containing 8.3 mM glucose and 7.0 mM amino acids). When stimulated by buffer B, the amount of insulin secreted increased (P less than 0.05) from immaturity (2 mo) to adulthood (10-18 mo) because of growth of the organ. From adulthood to very old age an equal amount of insulin was released in all groups during the last 19 min of perfusion with buffer B. Fasting blood glucose levels remained constant throughout life, whereas pancreatic insulin stores and plasma insulin levels rose, reaching peak values at 18 mo. The alpha-cell appeared to be deemphasized relative to the beta-cell during development but not thereafter, as indicated by the findings that from immaturity to adulthood pancreatic glucagon stores expanded less than insulin stores and that glucagon release significantly decreased. Only minor changes in somatostatin release from the delta-cells were observed after the rat reached adulthood. We conclude that the endocrine secretory response of the pancreas is well maintained throughout life in the Fischer 344 rat.


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